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The complex venous response to the ETB receptor (ETBR) agonist sarafotoxin S6C
Author(s) -
Szasz Theodora,
Watts Stephanie W
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb96-a
Subject(s) - contraction (grammar) , agonist , endothelin receptor , endocrinology , nitric oxide , medicine , chemistry , endothelium , aorta , vasodilation , anesthesia , receptor
Arteries and veins are both actively engaged in the control of cardiovascular function. However, they display many functional differences, such as the involvement in the endothelin system. In the endothelium, ET BR mediates nitric oxide (NO) release and relaxation, while on smooth muscle cells (SMCs) it mediates contraction. Although the ET BR is present on SMCs of both rat aorta (RA) and vena cava (RVC), stimulation with S6C, a selective ET BR agonist, leads to contraction of the RVC, but not RA. We hypothesized that the venous endothelial ET BR is less functionally active than the arterial one. Therefore we studied the ability of S6C to act as a relaxing agent when used on contracted, endothelium‐intact RA and RVC. In PGF2α (20 μM)‐contracted RA, S6C (100 nM) induced a relaxation (21.5±4.8% PGF2α‐induced contraction). By contrast, in the RVC, S6C induced a four‐phase response (short relaxation‐short contraction‐long relaxation‐long contraction). BQ788, the ET BR antagonist (1 μM), blocked the S6C‐induced relaxation in the aorta, while it only altered the short contractile phase of the VC response. The RVC response to S6C cannot be explained by a different ability of venous and arterial endothelium to produce NO, since ACh (10 μM) induced a similar relaxation of RA and RVC, which was completely blocked by LNNA (100 μM). These data highlight increasingly complex functions of the ET BR in the cardiovascular system.